An effect of glucocorticoids to antagonize insulin effects upon glucose transport is well known. As the mechanism of action of insulin is not well understood, however, it has not been possible to determine the mechanism by which corticosteroids produce this effect. Many studies by other workers have indicated that changes in the fat cell membrane appear to mimic the stimulation of glucose transport seen with insulin, but no changes in the proteins of plasma membrane vesicles isolated from adipose tissue cells treated with insulin could be demonstrated by infra-red spectroscopy or fluorescent probe studies. It has been shown that changes in the membrane phospholipids by treatment with phospholipase C stimulates glucose metabolism. Recent studies in this laboratory have demonstrated an effect of dexamethasone to change the phospholipid composition of fat cell membranes. It is proposed to investigate whether these changes in the phospholipids of the fat cell membrane are responsible for the inhibition of insulin effects upon glucose transport produced by glucocorticoids and also to relate these changes to the effect of corticoids on the lipolytic action of epinephrine. Studies will be carried out to determine whether insulin also produces changes in membrane phospholipids and whether the combination of glucocorticoids and insulin produce effects which are different from those of corticoid alone. Glucose transport will be measured with the 2-deoxy glucose methods developed by Olefsky and others and phospholipids will be determined by standard methods.